The effect of 4-pentenoic acid on fatty acid oxidation

Brendel, Klaus; Corredor, Carlos; Bressler, Rubin

doi:10.1016/0006-291x(69)90838-9

Cited by 37 publications

(16 citation statements)

References 8 publications

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“…Bressler and coworkers [36] observed that addition of CoA and carnitine together would overcome inhibition of fatty acid oxidation produced in pigeon liver homogenates and mitochondria by pentenoate, and under these conditions there was accumulation of pentenoyl-carnitine and acrylyl-carnitine. Similar results have not been published for MCPA.…”

Section: Metabolic Actionsmentioning

confidence: 99%

Biochemistry of hypoglycin

Manchester

1974

FEBS Letters

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Hypoglycin A, P_(methylenecyclopropyl)alanine, is a non-protein amino acid first isolated [l] from the unripe fruit of the ackee, Blighia sapida, a tree much cultivated in Jamaica where the fleshy aril constitutes an important item of diet, particularly of the lower income groups. The unripe ackee aril may contain around 1 mg of hypoglycin per g wet weight and the seeds two to three times as much, but as the fruit ripens the content of the aril decreases to less than 0.01% of the amino acid [2] . Hypoglycin is found in the seeds both as the free amino acid and the y-glutamyl dipeptide conjugate, hypoglycin B

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Section: Metabolic Actionsmentioning

confidence: 99%

Biochemistry of hypoglycin

Manchester

1974

FEBS Letters

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“…Pentenoic acid is a potent inhibitor of fatty acid oxidation (2,19). Bressler et al (3) has proposed that this inhibition is caused by depletion of intracellular free CoA and carnitine; however, Sherrat and coworkers (12), using isolated mito~hon-dria, have shown that there is no relation between the ability of related compounds to reduce mitochondria-free CoA and their ability to inhibit fatty acid oxidation.…”

Section: T E S T Control T E S T Control T E S T Controlmentioning

confidence: 99%

“…At higher concentrations it also impairs other mitochondrial functions (20). Pentenoic acid results in decreased tissue ATP and NADH (2,29). The reduced availability of energy probably accounts for the decreased gluconeogenesis (24).…”

Section: T E S T Control T E S T Control T E S T Controlmentioning

confidence: 99%

Production of the Features of Reye's Syndrome in Rats with 4-Pentenoic Acid

1975

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IN VIVO D-GLUCOSE(1 l), in perfusion studies of the proximal intestine, found rate of absorption of glucose to be about 10 mg/hr/lO cm. In the present study, rate of absorption from a solution with a similar mean glucose concentration was 8 mg/hr/lO cm of the perfused jejunum + ileum. SUMMARYIn vivo study of D-glucose absorption in small intestine of rats between 7 and 73 days of age suggested that rate of absorption normalized for intestinal weight incre'ased twofold at the time of weaning (21-23 days of age) with no further increase thereafter. REFERENCES AND NOTES

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“…Pent-4-enoate is usually regarded as an inhibitor of the fl-oxidation of fatty acids (Corredor et al, 1967;Senior & Sherratt, 1978a,b;Senior et al, 1968;Brendel et al, 1969;Fukami & Williamson, 1971). Its effects seem to be tissue-specific, however.…”

mentioning

confidence: 99%

Effects of pent-4-enoate on cellular redox state, glycolysis and fatty acid oxidation in isolated perfused rat heart

Hiltunen

Jauhonen

Savolainen

et al. 1978

Biochemical Journal

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The metabolic effects of pent-4-enoate were studied in beating and potassium-arrested perfused rat hearts. The addition of 0.8imM-pent-4-enoate to the fluid used to perfuse a potassium-arrested heart resulted in a 70 % increase in the 02 consumption and a 66 % decrease in the glycolytic flux as measured in terms of the de-tritiation of [3-3H]glucose, although the proportion of the 02 consumption attributable to glucose oxidation decreased from an initial 30 % to 10 %. The pent-4-enoate-induced increase in 02 consumption was only 15 % in the beating heart. In the potassium-arrested heart, pent-4-enoate stimulated palmitate oxidation by more than 100% when measured in terms of the production of "4CO2 from [1-14C]palmitate, but in the beating heart palmitate oxidation was inhibited. Perfusion of the heart with pent-4-enoate had no effect on the proportion of pyruvate dehydrogenase found in the active form, in spite of large changes in the CoASH and acetyl-CoA concentrations and changes in their concentration ratios. The effects of pent-4-enoate on the cellular redox state were dependent on the ATP consumption of the heart. In the beating heart, pent-4-enoate caused a rapid mitochondrial NAD+ reduction that subsequently faded out, so that the final state was more oxidized than the initial state. The arrested heart, however, remained in a more reduced state than initially, even after the partial re-oxidation that followed the initial rapid NAD+ reduction. The ability of pent-4-enoate to increase or decrease fatty acid oxidation can be explained on the basis of the differential effects of pent-4-enoate on the concentration of citric acid-cycle intermediates under conditions of high or low ATP consumption of the myocardial cell. The proportion of the fatty acids in the fuel consumed by the heart is probably primarily determined by the regulatory mechanisms of glycolysis. When pent-4-enoate causes an increase in the citric acid-cycle intermediates, feedback inhibition of glycolysis results in an increase in the oxidation of fatty acids.

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The effect of 4-pentenoic acid on fatty acid oxidation

Cited by 37 publications

References 8 publications

Biochemistry of hypoglycin

Biochemistry of hypoglycin

Production of the Features of Reye's Syndrome in Rats with 4-Pentenoic Acid

Effects of pent-4-enoate on cellular redox state, glycolysis and fatty acid oxidation in isolated perfused rat heart

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